Search PubMed⌕ Search

Biomedical subjects

R Kiss

Publications and source records attributed to R Kiss.

At least 253 records · Page 14Linked to original sources
PubMed1988

Lectins in histochemistry. A survey.

The most pertinent works using lectin histochemistry at both light and electron microscopy were reviewed. The results and their eventual interpretation are summarized. The importance of lectins as a histochemical tool is mainly based upon the two following features: they possess a narrow specificity for various carbohydrate residues and they can be linked to different labels (fluorochrome, peroxidase, ferritin, colloidal gold) or be included in immunocytochemical techniques in order to be visualized at conventional, u.v. and electron microscopes. These have the advantage to preserve the cellular and tissular integrity. Various tissues and organs were investigated first as a descriptive manner and then under cell differentiation and ontogenetic points of view. Tissues from laboratory rodents and human were especially studied. Few works regarding other vertebrates have been published. However comparative studies could probably cast some lights regarding functions and phylogenetic evaluation. Finally, lectin histochemistry in pathology seems of great promise as indicated by the growing number of publications.

Animals↗
PubMed1988

Treatment of heart failure associated with acute and chronic forms of ischaemic heart disease by captopril (Tensiomin, EGIS).

The effect of oral Tensiomin treatment, 53.4 mg daily in 29 patients suffering from congestive heart failure associated with acute of chronic forms of ischaemic heart disease, e.g., recent and/or advanced myocardial infarction, aneurysm etc. was studied. The acute and long-term beneficial haemodynamic effects were verified in 4 patients by thermodilution Swan-Ganz catheterization as well. The parameters of ejection function improved moderately, while left ventricular filling pressure (PCW) decreased significantly. The balanced vasodilator effect was not accompanied by an increased myocardial oxygen demand. The "double product" was lowered in response to Tensiomin. During the clinical follow-up (from 6 days to 2 years) there was an improvement in the NYHA functional class by an average of 1.2 however 4 patients died in spite of combined vasodilator and dobutamine treatment. Owing to the improvement of regional blood flow to the brain and the kidney Tensiomin seems to be well-tolerated in patients with low arterial blood pressure. In pts with acute myocardial infarction and angina the critical fall of blood pressure and that of the coronary blood flow should be avoided by giving the drug in approximately titrated. Side effects were observed only with higher doses of Tensiomin in a small number of patients, i.e., transient worsening of renal function in 3 patients and dysgeusia in 2. Our data indicate that Tensiomin treatment is effective and safe in patients suffering from all kinds of congestive heart failure complicating ischaemic heart disease.

Aged↗
PubMed1987

Effect of ovariectomy, hypophysectomy and/or GnRH analog (HRF) administration on the cell proliferation of the MXT mouse hormone-dependent mammary tumor.

The MXT tumor is an experimental mammary neoplasm which is maintained by serial transplantation using B6D2F1 mice, and which contains significant amounts of estrogen and progesterone receptors. The aim of the present study is to examine the effects of ovariectomy (OVX) or ovariectomy plus hypophysectomy (OVX-HX) on both the macroscopic growth and the cell proliferation of this tumor. This cell proliferation was evaluated by means of in vivo tritiated thymidine autoradiography. In addition, we investigated the effects of a GnRH analog (Gonadorelin: HRF, 5-oxo-Pro-His-Trp-Ser-Tyr-Gly-Leu-Arg-Pro-Gly-hydrochloride) on MTX tumor cell proliferation on 7 day-OVX and 5 day-HX (OVX-HX) mice. The uterine luminal epithelium was chosen to monitor the methodology. Our data clearly demonstrate that there is a delay in the growth of MXT tumors grafted into hypophysectomized animals and, to a lesser degree, ovariectomized animals. With respect to proliferation, castration induced a dramatic decrease of the thymidine labelling index (TLI) in the tissue used to monitor the methodology (the uterine luminal epithemium); in contrast, no cell proliferation was induced by hypophysectomy or HRF administration. In 4-week-old MXT tumors, ovariectomy also markedly decreased the TLI within a few days of its taking place. However hypophysectomy, performed on castrated animals, induced a significant and transient increase of cell proliferation in this neoplasm, an increase which lasted from the 2nd to the 5th day following the operation. The high basal level of MXT cell proliferation recorded in OVX-HX animals decreased dramatically after the administration of HRF between 12 and 48 h prior to the sacrifice of the animals. It is concluded that the HRF exerts a direct effect on the MXT tumor cells, and this HRF might be essential for their growth.

Animals↗
PubMed1987

In vitro studies of canine mammary tumors: influence of 17-beta-estradiol and progesterone on cell kinetics parameters.

Using an in vitro tritiated thymidine nuclear labeling followed by autoradiography, the effects of 17-beta-estradiol (E2) or progesterone (Pg) were studied in 30 canine mammary tumors that were incubated and hormonally stimulated in vitro. In 10 of these tumors, the synthetic (S) phase duration was also measured in absence or in presence of E2, by using a double labeling with tritiated thymidine. Our results demonstrate that E2, and, to a lesser degree, Pg can induce cell replication in both estrogen receptor-positive (ER+ PgR+) and estrogen receptor-negative (ER- PgR-) canine mammary tumors. The mitogenic effect of E2 may involve a shortening of the DNA S cell cycle phase. We have also found a significantly positive relationship between the estrogen and the progesterone receptor concentrations and the basal proliferation rate in these tumors, whereas no correlation was found between steroid receptor contents and the maximal level of stimulation achieved after E2 or Pg exposure.

Animals↗
PubMed1987

Immunohistochemical localization of atrial natriuretic peptide in primary aldosteronism.

Using the immunoperoxidase method with specific antibody, we examined the presence of atrial natriuretic peptide (ANP) in adrenal tissues of a patient with primary aldosteronism and those derived from a patient with Cushing's syndrome. We found cells immunopositive for ANP in primary aldosteronism but not in Cushing's syndrome. In primary aldosteronism, we noted positively stained cells mainly but not exclusively in the adenomatous tissue. These results demonstrate for the first time the presence of immunoreactive ANP in adrenal tissues of a patient with primary aldosteronism and suggest that adrenal ANP may have potentially important impacts on aldosterone secretion in this disorder.

Adrenal Glands↗
PubMed1987

Synergism or antagonism between estradiol and progesterone on the cell kinetic parameters of the MXT mouse mammary tumor.

With the use of an in vivo tritiated thymidine ([3H]dThd) nuclear labeling followed by autoradiography, the effects at different times before sacrifice of single or paired injections of 17 beta-estradiol (E2) and/or progesterone (Pg), at different concentrations, were studied in (C57BL x DBA/2f)F1 (B6D2F1) mice transplanted with the MXT hormone-sensitive mammary tumor. Uteri were chosen as controls for the methodology. With regard to MXT tumors, E2 (0.25, 2.50, or 25.00 micrograms/animal) or Pg (125, 600, or 5,000 micrograms/animal) exerts almost a similar mitogenic influence that is dose related to the former and nor for the later, at least within the range of concentrations studied here; and the mitogenic effect of Pg seems to appear earlier than that of E2. When these steroids are concomitantly given, no obvious synergistic or antagonistic effect can be observed. A second E2 administration seems to have a less pronounced effect on cell proliferation as compared to that exerted by the first injection performed 12 or 24 hours earlier. On the contrary, the repetition of a Pg treatment would rather exert an additive or even a synergistic effect on the tumoral dThd labeling indices with regard to the total duration of stimulation. When one of these two steroids is administered first, it blocks totally the mitogenic effect of the second, provided the latter is given 24 hours later. It is concluded that E2 and Pg have almost a similar mitogenic effect on the MXT tumor and that these hormones exert complex interactions that are probably very important for the growth regulation of this cancer. Further investigations are needed to better understand the precise biochemical mechanisms involved in the modulating actions of these steroids on the MXT mammary growth.

Animals↗
PubMed1987

Effect of prolactin and estradiol on cell proliferation in the uterus and the MXT mouse mammary neoplasm.

With the use of an in vivo tritiated thymidine [( 3H]dThd) nuclear labeling followed by autoradiography, the effects at different times before sacrifice of prolactin (PRL) and/or 17 beta-estradiol (E2) were studied in C57BL X DBA/2f)F1 mice given transplants of the MXT hormone-sensitive mammary tumor whose growth was previously shown to be influenced by E2 and/or progesterone. Uteri were chosen as controls for the methodology. Experiments were conducted on ovariectomized mice submitted to endocrine manipulation to achieve plasma PRL modifications. In addition to E2, the proliferation of cancer cells, assessed by the measurement of thymidine labeling indices (TLIs), was demonstrated to be enhanced by ovine prolactin (oPRL) and Sulpiride and strongly slowed down by castration and 2-bromo-alpha-ergokryptin treatment, thus emphasizing the great importance of PRL in mammary cancer development. Moreover, a pulse of 1 mg oPRL/animal produced a marked TLI rise in tumors, lasting from the 6th to the 48th hour after its injection and reaching a maximum at 24 hours. PRL had no proliferative effect on the uterine luminal epithelium. When PRL and E2 were injected concomitantly, the profile of stimulation was quite similar to that obtained with E2 alone; i.e., a maximum stimulation was observed at the 24th and 36th hours after hormonal pulse. From these data it is concluded that, in spayed mice, not only E2 but also PRL is of major importance leading to enhanced proliferation of MXT mammary neoplastic cells. Further investigations are needed to throw light on the cellular events presiding over the action of PRL and E2 at the cancer cell level.

Animals↗
PubMed1986

Morphology of MXT mouse mammary tumors. Correlation with growth characteristics and hormone sensitivity.

The transplantable MXT mouse mammary tumor has been a useful tool for studying endocrine mechanisms underlying mammary tumor growth. It is our experience, however, that this model is unstable during serial transplantation. This paper analyses this variability from the viewpoints of histology and estrogen receptor content and indicates that these parameters should always be checked before planning experimental work. It is advised that a more homogeneous material is needed and that this goal should be achieved by clonal selection before transplantation.

Animals↗
PubMed1986

Sensitivity of the hormone dependent MXT-mouse mammary carcinoma to estradiol during tumoral growth. An autoradiographic study.

The MXT transplantable mammary tumor is an ovarian sensitive carcinoma of the B6D2F1 mouse strain. The present work documents the mitogenic effect of a single near-physiological dose (pulse) of estradiol (E2) in castrated mice bearing MXT neoplasms 2-7 weeks after their inoculation. Histological sections of tumors and uteri (as control E2 target organs) were processed and nuclear thymidine labeling indices (TLI) were determined by autoradiography. Tumor estrogen receptors contents were evaluated in parallel. The results indicate that the MXT tumor keeps a constant sensitivity to E2 6 weeks after implantation.

Animals↗
PubMed1986

Effect of progesterone on cell proliferation in the MXT mouse hormone-sensitive mammary neoplasm.

The transplantable MXT mouse mammary tumor is an experimental model for which the growth is modulated by ovarian hormones; because of scant knowledge about the effects of progesterone (Pg) alone on cancer cells, the present investigation was made. By measuring the percentage of cells with labeled nuclei after tritiated thymidine ([3H]dThd) injection 1 hour prior to sacrifice [dThd labeling index (TLI)], a study was made of the effect (in vivo) of a near physiologic dose of Pg (125 micrograms ip) on cell proliferation in uteri (as the control Pg target organ) and on tumors of spayed (C57BL female X DBA/2F male)F1 mice. Pg induced a significant and transient rise in TLI, which increased from the 12th to the 24th hour after its injection. This mitogenic effect on tumors was comparable to that elicited by 0.25 microgram 17 beta-estradiol injected under similar conditions. In vivo brief exposure of castrated mice to Pg induced a significant mitogenic effect on MXT tumors. These observations might have important consequences for a better understanding of the endocrine mechanisms involved in human hormone-dependent breast cancer.

Adenocarcinoma↗
PubMed1985

Histological staining by tritiated actinomycin D: a useful tool to study neoplastic cell heterogeneity and estrogen sensitivity of mammary tumors.

The MXT mouse transplantable mammary cancer is characterized by significant amounts of steroid hormone receptors. Moreover this model, as other solid tumors, contains diverse subpopulations of neoplastic cells. In the present study we have examined this pattern as well as the influence of exogenous physiologic doses of estradiol on tumor cell subpopulations. Their identification was undertaken at the morphological level employing incubation of tritiated actinomycin D with fixed material followed by autoradiography. This semiquantitative cytochemical method has proved itself to be a useful tool in order to assess the cellular heterogeneity of carcinoma cells.

Animals↗
PubMed1985

Effect of castration and 17 beta-estradiol pulse on cell proliferation in the uterus and the MXT mouse mammary tumor.

The effects of a single 17 beta-estradiol (E2) injection on cell proliferation were studied in 3 groups of 30 mice transplanted with the MXT ovary-dependent mammary tumor. In group A, all animals were castrated prior to tumor implantation; groups B and C had intact ovaries at the time of transplantation, but group B was left intact throughout the experiment, while group C underwent castration 4 weeks later. On day 40 in groups B and C and on day 80 in group A, in which tumor development was significantly delayed, the same procedure for testing the effects of E2 was applied: Ten controls received 0.1 ml saline ip and were killed on the next day; 4 lots of 5 mice received 0.25 micrograms E2 ip and were killed one by one at 12-hour intervals. Exactly 1 hour prior to sacrifice, each animal received 25 microCi [methyl-3H]thymidine ip. Histologic sections of tumors and uteri were processed for autoradiography, and nuclear thymidine (dThd) labeling indices (LI) were determined. All tumors of group A grafted under unfavorable hormonal conditions were poorly differentiated, and E2 injection induced no appreciable changes in their dThd LI. Tumors B and C were well-differentiated adenocarcinomas, in which E2 induced significant modifications of cell proliferation. In group B, complex changes in dThd LI occurred in tumors as well as in uteri, probably due to interferences with the ovarian hormonal production. In group C, E2 produced a marked rise in dThd LI in tumors, lasting from the 12th to the 36th hour after its injection. Stimulation was maximum at the 24th hour, representing a 2.8-fold increase over mean basal dThd LI. It is concluded that the presence of an intact ovarian function at the time of transplantation is critical for maintaining the properties of hormone dependence in MXT tumors. In mice castrated after tumor implantation, a single E2 injection induces a marked and partially synchronous proliferation of neoplastic cells. The hypothesis that such hormonal manipulation might amplify the killing effect of cell cycle- or phase-specific cytotoxic drugs could be adequately tested with this model.

Adenocarcinoma↗